4. ANALYSIS O F FACTORS INVOLVED I N SYMBIOSIS
65
been randomly reported in the literature, more or less as afterthoughts.
A survey of the literature has revealed the following reports. Mackin
( 1951) has reported that in Dermocystidium-infected Crassostrea
virginica abscesses are formed of which the outer margins are composed
of phagocytes, other hemocytes (?), and some fibrous connective
tissue. Newton (1952, 1954), working with experimental infections of
Puerto Rican and Brazilian strains of Australorbis glabratus by Puerto
Rican Schistosoma mansoni, has found that the Puerto Rican snails,
when exposed to miracidia, yield 95%infection while none of the Brazilian
snails become infected. Histological examination of the Brazilian snails
has revealed a rapid tissue reaction, occurring within 48 h, where there
are marked cellular infiltrations around the miracidia. This is followed
by a fibrotic type of encapsulation and degeneration of the parasites.
Studies on the susceptibility of the progenies, resulting from crossing
the Puerto Rican and Brazilian strains of Australorbis glabratus, have
revealed that the susceptibility, i.e. the presence and efficiency of the
encapsulation phenomenon, is genetically controlled, involving several
factors. Inheritance, however, does not appear to be the sole determining factor, since Newton (1953) has also been able to demonstrate
that young snails (1-4 weeks old) of the Brazilian strain are susceptible
and will sustain the growth of Schistosoma mansoni larvae of the
Puerto Rican strain. Subsequently, El Gindy (1954) and Moore et al.
(1953) have confirmed that the susceptibility of snailsis influenced by age
although apparently this does not hold true in all species (see Stunkard,
1946 ; Abdel-Malek, 1950 ; Kagan et al., 1954).
Brooks (1953) has also reported the occurrence of encapsulation in
unnatural hosts. It was reported that 8. mansoni miracidia will penetrate A . glabratus, its normal host, and Tropicorbis havanensis, an
unnatural host, in approximately the same number ; however, in T.
havanensis, encapsulation of the majority of the miracidia, involving
cellular proliferation and infiltration, occurs within 24 h and the
parasites die within 3 days. As the intramolluscan stages of trematodes
are generally believed not to elicit encapsulation in their natural hosts
(see review of pathological changes in trematode-parasitized molluscs
by Cheng and Snyder, 1962a), Sudds (1960), utilizing this assumption
as his working hypothesis, has tested the compatibility or incompatibility of four species of schistosomes (Trichobilharzia elvae, T.
physellae, Schistosonaatium douthitti and Schistosoma mansoni) with
twenty-six species of gastropods. He has found that the four species
of miracidia will attempt to penetrate all of the natural hosts and the
majority of the unnatural hosts. Subsequent histological examinations
revealed that miracidia in natural hosts develop normally, without
A.M.B.--G
0
65
been randomly reported in the literature, more or less as afterthoughts.
A survey of the literature has revealed the following reports. Mackin
( 1951) has reported that in Dermocystidium-infected Crassostrea
virginica abscesses are formed of which the outer margins are composed
of phagocytes, other hemocytes (?), and some fibrous connective
tissue. Newton (1952, 1954), working with experimental infections of
Puerto Rican and Brazilian strains of Australorbis glabratus by Puerto
Rican Schistosoma mansoni, has found that the Puerto Rican snails,
when exposed to miracidia, yield 95%infection while none of the Brazilian
snails become infected. Histological examination of the Brazilian snails
has revealed a rapid tissue reaction, occurring within 48 h, where there
are marked cellular infiltrations around the miracidia. This is followed
by a fibrotic type of encapsulation and degeneration of the parasites.
Studies on the susceptibility of the progenies, resulting from crossing
the Puerto Rican and Brazilian strains of Australorbis glabratus, have
revealed that the susceptibility, i.e. the presence and efficiency of the
encapsulation phenomenon, is genetically controlled, involving several
factors. Inheritance, however, does not appear to be the sole determining factor, since Newton (1953) has also been able to demonstrate
that young snails (1-4 weeks old) of the Brazilian strain are susceptible
and will sustain the growth of Schistosoma mansoni larvae of the
Puerto Rican strain. Subsequently, El Gindy (1954) and Moore et al.
(1953) have confirmed that the susceptibility of snailsis influenced by age
although apparently this does not hold true in all species (see Stunkard,
1946 ; Abdel-Malek, 1950 ; Kagan et al., 1954).
Brooks (1953) has also reported the occurrence of encapsulation in
unnatural hosts. It was reported that 8. mansoni miracidia will penetrate A . glabratus, its normal host, and Tropicorbis havanensis, an
unnatural host, in approximately the same number ; however, in T.
havanensis, encapsulation of the majority of the miracidia, involving
cellular proliferation and infiltration, occurs within 24 h and the
parasites die within 3 days. As the intramolluscan stages of trematodes
are generally believed not to elicit encapsulation in their natural hosts
(see review of pathological changes in trematode-parasitized molluscs
by Cheng and Snyder, 1962a), Sudds (1960), utilizing this assumption
as his working hypothesis, has tested the compatibility or incompatibility of four species of schistosomes (Trichobilharzia elvae, T.
physellae, Schistosonaatium douthitti and Schistosoma mansoni) with
twenty-six species of gastropods. He has found that the four species
of miracidia will attempt to penetrate all of the natural hosts and the
majority of the unnatural hosts. Subsequent histological examinations
revealed that miracidia in natural hosts develop normally, without
A.M.B.--G
0